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http://scihub22266oqcxt.onion/ C4440051!4440051 !26045742     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26045742 &cmd=llinks): Failed to open stream: HTTP request failed! 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Neuroprotective effect of fasudil on inflammation through PI3K/Akt and Wnt/?-catenin dependent pathways in a mice model of Parkinson s disease |pdf=|usr=}}{{26045742 }} gab.com Text Neuroprotective effect of fasudil on inflammation through PI3K/Akt and Wnt/ -catenin dependent pathways in a mice model of Parkinson s disease JO: Int J Clin Exp Pathol http://www.kidney.de/pget.php?&tw=1&pmid=26045742 #FOAvip OBJECTIVE: Fasudil, a Rho kinase inhibitor, has neuroprotection in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-based Parkinson's disease (PD). This study aims to investigate the mechanism underlying the neuroprotection of fasudil in the PD mice model. METHODS: Female MPTP-intoxication C57BL/6 mice were treated with normal saline or fasudil on day 15 after first administration of MPTP. Pole test was used for the behavioral analysis of mice. Expression of interleukin-1? (IL-1?) and tumor necrosis factor alpha (TNF-?) in brain tissue were detected by ELISA. Expression of tyrosine hydroxylase (TH), p-MYPT1, p-nuclear transcription factor NF-?B, toll-like receptor 2 (TLR2), arginase1, inducible nitric oxide synthase (iNOS), bromodeoxyuridine (BrdU), glial cell line-derived neurotrophic factor (GDNF), p-GSK-3b, p110-PI3K, p-Akt, WNT1, Fzd1 and ?-catenin were determined by western blot and immunofluorescence analysis. RESULTS: Fasudil enhanced the number of TH neurons which was decreased by MPTP treatment. Behavioral test showed that the motor performance of mice was improved after fasudil treatment. The expression of IL-1?, TNF-?, TLR2 and p-NF-?B and iNOS were lower after fasudil treatment (P<0.05) while the expression of arginase1 was increased (P<0.05). Further, we could observe the increase of GDNF expression in the microglial cells. The expression of p110-PI3K, p-Akt, WNT1, Fzd1 and ?-catenin were increased after fasudil administration (P<0.05) in MPTP-based mice model. CONCLUSIONS: Maybe fasudil protect dopamine neurons from loss in the MPTP mice model of PD through inflammatory inhibition via activation of PI3K/p-Akt and WNT1/Fzd1/?-catenin cell signaling pathways. Twit Text FOAVip Neuroprotective effect of fasudil on inflammation through PI3K/Akt and Wnt/ -catenin dependent pathways in a mice model of Parkinson s disease ????Int J Clin Exp Pathol http://www.kidney.de/pget.php?&tw=1&pmid=26045742 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26045742 #FOAvip English Wikipedia <ref>{{Cite pmid|26045742 }}</ref> Neuroprotective effect of fasudil on inflammation through PI3K/Akt and Wnt/?-catenin dependent pathways in a mice model of Parkinson s disease #MMPMID26045742 Zhao Y ; Zhang Q ; Xi J ; Xiao B ; Li Y ; Ma C Int J Clin Exp Pathol 2015[]; 8 (3 ): 2354-64 PMID26045742 show ga OBJECTIVE: Fasudil, a Rho kinase inhibitor, has neuroprotection in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-based Parkinson's disease (PD). This study aims to investigate the mechanism underlying the neuroprotection of fasudil in the PD mice model. METHODS: Female MPTP-intoxication C57BL/6 mice were treated with normal saline or fasudil on day 15 after first administration of MPTP. Pole test was used for the behavioral analysis of mice. Expression of interleukin-1? (IL-1?) and tumor necrosis factor alpha (TNF-?) in brain tissue were detected by ELISA. Expression of tyrosine hydroxylase (TH), p-MYPT1, p-nuclear transcription factor NF-?B, toll-like receptor 2 (TLR2), arginase1, inducible nitric oxide synthase (iNOS), bromodeoxyuridine (BrdU), glial cell line-derived neurotrophic factor (GDNF), p-GSK-3b, p110-PI3K, p-Akt, WNT1, Fzd1 and ?-catenin were determined by western blot and immunofluorescence analysis. RESULTS: Fasudil enhanced the number of TH neurons which was decreased by MPTP treatment. Behavioral test showed that the motor performance of mice was improved after fasudil treatment. The expression of IL-1?, TNF-?, TLR2 and p-NF-?B and iNOS were lower after fasudil treatment (P<0.05) while the expression of arginase1 was increased (P<0.05). Further, we could observe the increase of GDNF expression in the microglial cells. The expression of p110-PI3K, p-Akt, WNT1, Fzd1 and ?-catenin were increased after fasudil administration (P<0.05) in MPTP-based mice model. CONCLUSIONS: Maybe fasudil protect dopamine neurons from loss in the MPTP mice model of PD through inflammatory inhibition via activation of PI3K/p-Akt and WNT1/Fzd1/?-catenin cell signaling pathways. |1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine/*analogs & derivatives/pharmacology [MESH] |1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine [MESH] |Animals [MESH] |Anti-Inflammatory Agents/*pharmacology [MESH] |Behavior, Animal/drug effects [MESH] |Brain/*drug effects/enzymology/pathology/physiopathology [MESH] |Cell Survival/drug effects [MESH] |Class I Phosphatidylinositol 3-Kinases/*metabolism [MESH] |Cytokines/metabolism [MESH] |Disease Models, Animal [MESH] |Dopaminergic Neurons/*drug effects/enzymology/pathology [MESH] |Enzyme Activation [MESH] |Female [MESH] |Frizzled Receptors/metabolism [MESH] |Inflammation Mediators/metabolism [MESH] |Mice, Inbred C57BL [MESH] |Motor Activity/drug effects [MESH] |Neuroprotective Agents/*pharmacology [MESH] |Parkinsonian Disorders/chemically induced/*drug therapy/enzymology/physiopathology/psychology [MESH] |Phosphorylation [MESH] |Protein Kinase Inhibitors/pharmacology [MESH] |Proto-Oncogene Proteins c-akt/*metabolism [MESH] |Wnt Signaling Pathway/*drug effects [MESH] |Wnt1 Protein/metabolism [MESH] |beta Catenin/*metabolism [MESH]Neuroprotective effect of fasudil on inflammation through PI3K/Akt and(epmc).pdf DeepDyve Pubget Overpricing